Nab-Paclitaxel related cystoid macular edema.

Objectives: Nab-paclitaxel is a chemotherapeutic drug used to treat various solid malignant tumors. It was conceived with a solvent free formulation to overcome toxicity events and hypersensitivity reactions associated with paclitaxel. However, it still carries ocular adverse effects. The present review examines nab-paclitaxel related cystoid macular edema (CME) and the available therapeutic options. Materials and Methods: The literature was reviewed on nab-paclitaxel related CME on published articles through January 2021 using the keywords "nab-paclitaxel "and "cystoid macular edema". Results: Bilateral CME is found in patients in treatment with nab-paclitaxel and causes considerable visual acuity decline. In ophthalmology multimodal imaging has an integral role in the diagnostic work up of patients and shows characteristic findings in nab-paclitaxel related CME. The case of a patient with treatment for bilateral CME is presented and analyzed. Conclusions: The preferred management strategy for nab-paclitaxel-related CME is drug cessation that leads to complete resolution of edema. When discontinuation of treatment is not possible due to the systemic conditions of patients, effective alternative therapeutic modalities are topical dorzolamide or steroidal treatment. Given the higher complication hazards of intravitreal therapy topical treatment should be preferred owing to comparable efficacy.

Arthrogenic human synovial cysts: immunohistochemical profile of interleukin-1beta, interleukin-6, tumour necrosis factor-alpha.

BACKGROUND: Synovial cysts are currently classified as degenerative lesions affecting the joint capsule or adjacent structures. MATERIALS AND METHODS: In our study we describe the results obtained in an immunohistochemical study comprising 18 patients with synovial cysts, performed to evaluate the pathophysiological role of some inflammatory cytokines such as: interleukin (IL)-1ß, IL-6 and tumour necrosis factor-alpha (TNF-α). RESULTS: Results showed an over-expression of TNF-α, IL-1ß and IL-6 which appears to be involved in the onset and progression of the disease. At the present time it is not possible to affirm that these molecules play a direct role also due to the absence of further and more specific investigations. The authors therefore hypothesize that inhibition of inflammation may have a significant role in the pathogenesis and regression of synovial cysts. CONCLUSIONS: Hence, these inflammatory cytokines may be considered potential therapeutic targets. The development of synthetic inhibitors of these inflammatory factors could lead to a reduction in the intensity of inflammation, thus inhibiting the onset and development of the disease.